These studies involve the interaction of humoral antibodies with lymphocytes to affect tumor cell destruction and basic mechanisms of the influence of antibodies on cell-mediated immunity. We propose to raise antibodies against monoclonal anti-M-MuSV antibodies to determine if we can induce antitumor immunity using these anti-idiotypic antibodies. Lymphocytes bind IgM complexes in the presence Mg ions but no Ca ions. Macrophages bind IgM complexes in the presence of Ca ions but not Mg ions. In contrast, IgG binds to both independently of divalent cations. Human (Fc) 5 mu is being radiolabeled to evaluate its' binding different subpopulations of lymphocytes. C3 receptor bearing T cells appear in mouse thymus following M-MuSV infection. We will evaluate functional capabilities of C3 receptor bearing T cells and their Ly phenotype. The cells able to lyse antibody-sensitized target cells include T cells. The cells in the thymus possessing the lowest amount of thy 1.2 were the highest in their lytic capacity against antibody sensitized target cells. We will determine the Ly phenotype of the active K cells in the thymus. In a hapten-carrier system IgM anti-carrier potentiates helper activity and IgG anti-carrier produces suppressor activity. T cells are required for the IgM dependent helper activity. These data contribute to our understanding of the interaction of humoral antibodies with T cell-mediated immune functions. Some T cell-mediated events can be directed by humoral antibodies. We may be able to activate patients' own T lymphocytes against their tumor using the appropriate specific antibody.